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Biomedical subjects

N L Stephens

Publications and source records attributed to N L Stephens.

At least 73 records · Page 4Linked to original sources
PubMed1991

Echocardiographic indices and their relationship to the blood pressure response to ergometric exercise in apparently healthy men.

The relationship between atrial and ventricular echocardiographic abnormalities and ergometric exercise systolic blood pressure was studied in 77 apparently healthy men, of whom the majority (77%) were normotensive (resting blood pressure less than 140/90 mmHg), and the remainder (23%) borderline hypertensive (resting systolic blood pressure 140 to 159 mmHg and/or diastolic blood pressure 90 to 95 mmHg). Four categories of exercise systolic blood pressure were defined (less than 190, 190 to 199, 200 to 209 and greater than or equal to 210 mmHg). Left ventricular mass and left atrial dimension were measured by M-mode echocardiography and divided by body surface area to derive the left ventricular mass index and the left atrial dimension index. The prevalence of left ventricular hypertrophy, defined as a left ventricular mass index greater than or equal to 125 g/m2, was 11%. Two key findings were the much higher prevalence of left atrial enlargement, defined as left atrial dimension index greater than or equal to 2 cm/m2 at 23%, and the fact that left atrial enlargement occurred in the absence of left ventricular hypertrophy in the majority of subjects, whereas occurrence of left ventricular hypertrophy in the absence of left atrial enlargement was rare. This is consistent with the view that left atrial enlargement is a common precursor of left ventricular hypertrophy. Multivariate analysis showed exercise systolic blood pressure and cardiac index to be independent predictors of left atrial dimension index and left ventricular mass index (R2 for statistical models was 0.38 [P less than 0.0001] and 0.47 [P less than 0.0001], respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Cardiovascular adaptations to mechanical overload.

The cardiac changes resulting from mechanical overload of the left ventricle have been well documented and a variety of compensatory mechanisms described. These include a decrease in maximum velocity (V0) of shortening in the absence of reduction in active tension (P0), and a reversible decrease in myofibrillar adenosine triphosphatase activity resulting from isoenzymic shift from, predominantly, a form of myosin with high ATPase activity (V1) to another with low (V3). The thermodynamic advantage of the transition is the hypertrophied muscle possesses a more energy-efficient form of contraction. These reversible transitions resulted from altered gene expression of isoenzymic forms of myosin heavy chain. It must be borne in mind that the adaptational modifications just described appear to occur only in smaller animals such as the rat, that possesses several myosin isozymes. In large mammals it is mainly the V3 form of myosin that is present, which does not change with altered contractile state. Responses of the large arteries to hypertension have been poorly studied. This is surprising when one recalls that degenerative disease of such vessels, that include the aorta, carotids and ileo-femoral arteries is almost an obligatory concomitant of hypertension. Such studies as have been carried out indicate that hyperplasia is specific for abdominal aortic stenosis while hypertrophy is found in aortic smooth muscle in rats with systemic hypertension. Mechanically, an increase in V0 with no change in P0 have been reported; an increase in myofibrillar ATPase activity was also reported. Though two myosin heavy chain isozymes have been found in aortic smooth muscle densitometry did not reveal any difference in distribution between tissues from control and hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Induction of rhythmic contraction in canine tracheal smooth muscle.

Na(+)-K+ ATPase activity of the canine tracheal smooth muscle membrane is responsible for the electrogenic pumping of Na+ and K+ ions. It has been shown that this activity results in muscle relaxation. Based on the results of the current study, we suggest that prolonged electrical stimulation induces increased Na(+)-K+ ATPase activity in isolated tracheal smooth muscle. Tracheal smooth muscle pretreated with prolonged electrical stimulation developed graded mechanical activity when subsequently treated with histamine, serotonin, acetylcholine, or 80 mM K+. This increased isometric tension was interrupted by rhythmic activity, which was elicited by histamine or serotonin but not by acetylcholine or 80 mM K+ stimulation. The spontaneous phasic activity was not inhibited by atropine or propranolol but was totally inhibited by 10(-6) M ouabain. These results suggested that the relaxation phase of rhythmic contraction in response to histamine and serotonin stimulation could be the result of stimulated Na(+)-K+ ATPase activity.

Animals↗
PubMed1990

Increased myosin phosphorylation in sensitized canine tracheal smooth muscle.

We have reported that the maximal velocity of shortening and myofibrillar adenosine triphosphatase (ATPase) activity of antigen-sensitized airway smooth muscle are higher than that of nonsensitized airway smooth muscle (Kong, S. K., R. P. C. Shiu, and N. L. Stephens. J. Appl. Physiol. 60: 92-94, 1986). To extend these studies, we attempted to determine whether the increased myofibrillar ATPase activity from sensitized airway smooth muscle was associated with either a change in distribution of two myosin heavy chain isozymes or an increase in myosin light chain phosphorylation. Myosin heavy chain isozymes from both control and sensitized airway smooth muscle were separated by 4% sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Gels were analyzed by densitometry, which indicated that isozyme band pattern of sensitized airway smooth muscle was not different from that of the control. The maximal levels of phosphorylated myosin light chain from whole cell homogenates of sensitized and control tracheal smooth muscles were 0.65 +/- 0.029 (n = 6) and 0.40 +/- 0.025 mol Pi/mol light chain (n = 6), respectively. The degree of phosphorylation of myosin light chain of sensitized airway smooth muscle was significantly higher than that of the control (P less than 0.05). This study also indicated that increased myofibrillar ATPase activity in sensitized tracheal smooth muscle was correlated with phosphorylation of myosin light chain.

Animals↗
PubMed1990

Contractile properties of bronchial smooth muscle with and without cartilage.

The majority of in vitro studies on airway smooth muscle have used the trachealis (TSM) as a convenient substitute for muscle from airways that constitute the flow-limiting segment. The latter are technically difficult to work with. However, because the site of maximum resistance to airflow is at the third to seventh generations of the bronchial tree, the trachealis preparation is of limited value. Length-tension and force-velocity properties were therefore studied at optimal length (lo) of canine bronchial smooth muscle (BSM) from which cartilage had been carefully removed. Normalized maximum isometric tension or stress (Po x 10(4) N/m2) for BSM was 7.1 +/- 0.19 (SE), which was similar to that of BSM with cartilage (BSM+C, 6.8 +/- 0.21) but lower than for TSM (18.2 +/- 0.81). At length greater than lo, the BSM+C was stiffer than the BSM. The values of maximum shortening capacity (delta Lmax), obtained directly from isotonic shortening at a load equal to the resting tension at lo, were 0.76 lo +/- 0.03, 0.41 lo +/- 0.02, and 0.24 +/- 0.02 lo for TSM, BSM, and BSM+C, respectively. The BSM and BSM+C delta Lmaxs were different (P less than 0.05). Maximal shortening velocities (Vo) for BSM, elicited at 2, 4, and 8 s by quick release in the course of an isometric contraction were significantly higher than for the BSM+C. Vos showed gradual decreases in all three groups in the later phase of contraction, suggesting the operation of latch bridges.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Mechanical alterations in sensitized canine saphenous vein.

Because it is likely that antigen sensitization is not restricted to airway smooth muscle but probably involves all tissues in the animal, we decided to test the hypothesis that saphenous vein from pollen extract-sensitized dogs is sensitized and is, in addition, mechanically altered. To this end, we studied responses to specific antigen challenge and length-tension and force-velocity relationships in sensitized (SSV) and control saphenous veins (CSV). The antigen challenge revealed that the venous smooth muscle was strongly sensitized and developed a Schultz-Dale response, the two main mediators of which were histamine and norepinephrine. Length-tension relationship studies showed that whereas there is no difference in maximum isometric tension development between SSV and CSV [93.95 +/- 7.34 and 87.86 +/- 4.00 (SE) mN/mm2, respectively], SSV exhibited a significantly greater maximum isotonic shortening capacity of 0.613 +/- 0.009 optional length (lo) vs. 0.578 +/- 0.012 lo for CSV. Unloaded shortening velocity (Vo), which reflects the cross-bridge cycling rate, was determined at different times after the onset of electrical stimulation. Maximum Vo was attained early (5 s) in the contraction; a 15% decline in Vo was observed at the plateau of the contraction (15 s). At 5 s, Vo of SSV (0.316 +/- 0.019 lo/s) was significantly higher than that of CSV (0.269 +/- 0.018 lo/s), although Vos were same at 15 (0.249 +/- 0.021 lo/s for SSV and 0.237 +/- 0.019 lo/s for CSV). The increase in shortening likely results from th e increase in the early cross-bridge cycling rate because our studies show that the bulk of shortening occurs in the first 5 s.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗
PubMed1990

The association between exercise blood pressure and the prevalence of ECG abnormalities.

The relationship between atrial and ventricular electrocardiographic abnormalities and exercise systolic blood pressure was studied in 246 male and 183 female subjects, of whom 199 males and 158 females were normotensive (resting blood pressure below 140/90 mmHg) and 47 males and 25 females were borderline hypertensive (resting systolic blood pressure 140 to 159 and/or diastolic blood pressure 90 to 99 mmHg). Subjects were classified into three groups according to systolic blood pressure during treadmill exercise (less than or equal to 180 mmHg, 180 to 199 mmHg and greater than or equal to 200 mmHg). With respect to atrial electrocardiographic abnormalities, the prevalence of abnormal values of the P-terminal force in lead V1 increased significantly with increased levels of resting exercise systolic blood pressure in males and females. The prevalence of electrocardiographic left ventricular hypertrophy, as reflected in abnormal values of one or more RS voltage indices, increased significantly with exercise systolic blood pressure in males but not in females. Males did not show a trend of increasing electrocardiographic left ventricular hypertrophy with increased resting systolic blood pressure means. In females, the significant difference between resting systolic blood pressure means and electrocardiographic left ventricular hypertrophy did not reflect a linear progression across resting systolic blood pressure categories. The significant association of the P-terminal force in lead V1 with exercise systolic blood pressure has not previously been reported. Although an association between left ventricular hypertrophy and exercise systolic blood pressure in hypertensives has been reported by others, the association seen in normotensive and borderline hypertensive males has not been reported previously.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Changes of tracheal smooth muscle stiffness during an isotonic contraction.

Stiffness of the series elastic component (SEC) of canine tracheal smooth muscle in isotonic contraction and relaxation was measured by applying small force perturbations to the muscle and measuring the resulting length perturbations. The quick, elastic length transient was taken as the change in length of the SEC (delta L). The force perturbation was a train of 10-Hz rectangular force waves varying from 0 to 10% maximum isometric tension (Po) in magnitude (delta P = 10% Po). Stiffness of the SEC was estimated by the ratio delta P/delta L. The change in SEC stiffness with respect to the change in muscle length was further studied by obtaining the stress-strain curves of the SEC at different muscle lengths using the load-clamping method. The clamps were applied at a fixed time (10 s after stimulation). Length of the muscle 10 s after contraction was controlled by the magnitude of the isotonic afterload. It was found that the apparent SEC stiffness increased as muscle length decreased. This stiffness increase is not likely due to an increase in the number of attached cross bridges, but it is probably due to the gradual diminution of the SEC length itself during muscle shortening.

Animals↗
PubMed1989

Ca2+-dependent facilitated shortening in isotonic contraction of trachealis muscle.

We compared isotonic shortening with isometric force generation as a function of external Ca2+ in 166 tracheal smooth muscle (TSM) strips from 27 mongrel dogs in vitro. Concentration-response curves were generated with muscarinic stimulation (acetylcholine, ACh), alpha-adrenergic receptor activation (norepinephrine after beta-adrenoceptor blockade, NE), serotonin (5-HT), and KCl-substituted Krebs-Henseleit solution. The concentrations of 5-HT causing half-maximal shortening (ECS50, 1.54 +/- 0.14 X 10(-7) M) and half-maximal active isometric tension (ECT50, 1.72 +/- 0.30 X 10(-7) M) were similar (P = NS). Likewise, ECS50 (21.9 +/- 0.7 mM) and ECT50, (22.0 +/- 0.9 mM) were similar for KCl. In contrast, facilitated isotonic shortening (i.e., greater isotonic shortening for comparable degrees of force generation) was elicited with ACh and NE for all levels of force generation between 15 and 85% of maximum and for all concentrations of ACh from 3 X 10(-8) to 3 X 10(-5) M (P less than 0.05 for all points). Facilitated isotonic shortening also was elicited for all concentrations of NE from 10(-8) to 10(-6) M (P less than 0.05 for all points). Removal of Ca2+ from the perfusate substantially reduced the potency of ACh (P less than 0.001) and abolished differences between ECS50 (2.23 +/- 0.28 X 10(-5) M) and ECT50 (2.50 +/- 0.46 X 10(-5) M, P = NS). We demonstrate that for comparable degrees of force generation, muscarinic and alpha-adrenergic receptor activation cause greater isotonic shortening than KCl or 5-HT and that this facilitated shortening is associated with the concentration of external Ca2+.

Acetylcholine↗
PubMed1989

Normally cycling and latch bridges in venous smooth muscle.

We have studied the mechanical properties of the crossbridges of canine saphenous venous smooth muscle during activation by electrical stimulation. A length-tension relationship study showed that at optimal length (1o) the maximum isometric tension (Po) developed was 87.9 mN/mm2. Resting tension at 1o was only 6% Po, which indicates a very compliant muscle. Active tension was observed at muscle lengths greater than 0.3 1o. The maximum shortening capacity was 0.65 1o. Force-velocity and series elastic characteristics were determined by the method of quick release to a set of load clamps applied during the course of an isometric contraction. The data were fitted by the hyperbolic Hill equation. Estimated maximum shortening velocity at zero load (Vo) an index of the crossbridge cycling rate) was 0.26 1o/s which was attained early in the contraction (5 s after the stimulation). A 11.9% decline in Vo was observed at the plateau of the contraction which occurred at 15 s. The stress (sigma)-strain (epsilon) curve for the series elastic component could be approximated by the equation sigma = B[exp(A epsilon)-1], where A = 76.51 (1/1o), B = 2.89 mN/mm2 at 5 s and A = 61.49 (1/1o), B = 1.85 mN/mm2 at 15 s. Like other smooth muscles, in general, saphenous vein develops considerable isometric tension and has a high shortening capacity but a low shortening velocity. The reduction in shortening velocity that occurs after 5 s in an isometric contraction is probably due to the development of so-called latch bridges.

Animals↗
PubMed1988

The effect of 2,3-butanedione monoxime (BDM) on smooth muscle mechanical properties.

2,3-Butanedione monoxime (BDM) has been reported to selectively block crossbridge interaction in skeletal and cardiac muscle and BDM has been shown to cause a dose-dependent decrease in smooth muscle maximum tension development (Po). With the relatively recent descriptions of at least two functionally different types of crossbridges (those recruited early in contraction and then fairly rapidly--within 30% of the muscles' contraction time--replaced by very slowly-cycling or "latch" crossbridges), it became important to know whether BDM is a specific inhibitor of one type of crossbridge or the other. In this study it was shown that 7.5 mM BDM had an even greater affect on maximum shortening ability (delta Lmax) having decreased the tracheal smooth muscle delta Lmax by 47%. BDM treatment did not alter "transition time (tT; defined arbitrarily as the time in contraction at which a functionally significant number of slowly-cycling bridges have replaced rapidly-cycling bridges)" in tracheal smooth muscle. Velocity of shortening early in contraction i.e. prior to tT, was decreased by 48%, while velocity late in contraction i.e. post tT, was not decreased with BDM treatment. BDM caused a decrease in maximum load bearing capacity, or maximum force potential (MFP), at all times in contracting tracheal smooth muscle. This investigation supports the suggestion that BDM inhibits crossbridge cycling rate in smooth muscle. In particular BDM appears to specifically inhibit rapidly-cycling crossbridges or their control as it has no apparent affect on cycling rate of very slowly-cycling or "latch" crossbridges in tracheal smooth muscle.

Animals↗
PubMed1988

Studies of arterial smooth muscle relaxation in younger (16-18 week) and older (28-31 week) spontaneously hypertensive rats.

Both isometric and isotonic relaxation rates have previously been reported to be decreased in caudal arterial and mesenteric resistance arterial smooth muscle from 16- to 21-week-old spontaneously hypertensive rats (SHR) compared with muscle from age-matched normotensive Wistar-Kyoto rats (WKY). An increased maximum velocity of shortening (Vmax) and an increased shortening ability (delta Lmax) have also been reported for arterial smooth muscle from 16- to 21-week-old SHR. It has been suggested that both increased narrowing and prolonged narrowing of arteries contribute to the development of hypertension. However, SHR Vmax is not different from WKY Vmax when studying arterial muscle from older (28- to 31-week-old) rats. Thus increased arterial narrowing ability cannot be a contributing factor to the maintenance of hypertension. In this study the role of relaxation rate in the maintenance of hypertension was examined by comparing the relaxation rates of isometric and isotonic contractions of caudal arterial strips from 16- to 21-week-old SHR (n = 9) and WKY (n = 8) and from 28- to 31-week-old SHR (n = 7) and WKY (n = 5). While relaxation rates were lower for 16- to 21-week-old SHR compared with age-matched WKY preparations for both isometric and isotonic contractions, only isometric relaxation rates were found to be different in 28- to 31-week-old SHR compared with 28- to 31-week-old caudal arterial muscle (p less than 0.05). Vmax tended to normalize from a once-elevated velocity, while isometric relaxation rate remained decreased in SHR with ageing and (or) with progression of the hypertensive condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Velocity-length-time relations in canine tracheal smooth muscle.

Zero-load velocity (V0) as a function of the length of canine tracheal smooth muscle was obtained by applying zero-load clamps to isotonically contracting muscle under various loads. The load clamps were applied at a specific time after onset of contraction. The magnitude of the isotonic load therefore determines the length of the muscle at the moment of release or at the moment the unloaded shortening velocity was measured. A family of such V0-muscle length (L) curves was obtained at 1-s intervals in the time course of contraction. The V0-L curve was fitted by a parabolic function with satisfactory goodness of fit. The maximum shortening velocity at optimum muscle length varied with time, but the minimum length at which V0 diminished to zero was time independent.

Animals↗
PubMed1988

Fatigue of mouse diaphragm muscle in isometric and isotonic contractions.

Fatiguabilities of mouse diaphragm muscle in vitro in isometric and isotonic contractions were compared in this study. Isolated mouse diaphragm muscle was stimulated repetitively to induce fatigue during both isometric and isotonic contractions. The supramaximal electrical stimulation used was a train of 100-Hz, 0.5-ms pulses delivered to the muscle every 2 s for 0.5 s. The percentage decrease in isometric tension from beginning to end of the fatiguing process was used as the index of fatigue. The experiments were carried out at different PO2 levels in both normal and zero-glucose Ringer solutions. It was found that fatigue developed more rapidly in isotonic contractions than in isometric ones. Also, the extracellular glucose level demonstrated little effect on the muscle's short-term fatiguability, whereas reductions in the extracellular PO2 exerted a profound effect, especially in the case of isotonic fatigue.

Aerobiosis↗
PubMed1988

Sympathetic stimulation and hypertension in the pyridoxine-deficient adult rat.

Pyridoxal phosphate is the coenzyme of various decarboxylases involved in the formation of monoamine neurotransmitters such as gamma-aminobutyric acid, serotonin, dopamine, and norepinephrine. Adult male Sprague-Dawley rats placed on a pyridoxine-deficient diet for 8 weeks showed significant hypertension compared with pyridoxine-supplemented controls. Hypothalamic contents of pyridoxal phosphate, gamma-aminobutyric acid, and serotonin in the pyridoxine-deficient rats were significantly lower than those in pyridoxine-supplemented controls. Hypertension was associated with sympathetic stimulation. Treatment of pyridoxine-deficient rats with a single dose of pyridoxine (10 mg/kg body weight) reversed the blood pressure to normal levels within 24 hours, with concomitant restorations of hypothalamic serotonin and gamma-aminobutyric acid as well as the return of plasma norepinephrine and epinephrine to normal levels. Also, pyridoxine treatment reversed the hypothalamic hypothyroidism observed in pyridoxine-deficient rats. These results indicate an association between pyridoxine deficiency and sympathetic stimulation leading to hypertension.

Animals↗